# Double Emergency: A Case of Concurrent Heparin-Induced Thrombocytopenia and Acute Promyelocytic Leukemia

**Authors:** Anastasia Schuldt, Mohamed Samour

PMC · DOI: 10.7759/cureus.58927 · 2024-04-24

## TL;DR

A 48-year-old woman developed two rare blood disorders, heparin-induced thrombocytopenia and acute promyelocytic leukemia, at the same time and was successfully treated.

## Contribution

This case is novel as it highlights the rare co-occurrence of two hematologic emergencies requiring urgent and coordinated treatment.

## Key findings

- Both HIT and APL were confirmed through specific assays and responded to appropriate treatment.
- The patient's HIT resolved without bleeding or worsening thrombosis during anticoagulation.
- APL treatment with induction and consolidation led to no residual disease.

## Abstract

A 48-year-old woman presented to the hospital with acute pulmonary embolism in the setting of presumed apixaban failure and was transitioned to heparin. Rapidly progressive pancytopenia prompted workup with suspicion for heparin-induced thrombocytopenia (HIT) as well as peripheral blood smear concerning for acute promyelocytic leukemia (APL). She was emergently started on non-heparin anticoagulation and transferred to start APL-directed treatment. Both HIT and APL were confirmed with serotonin release assay (SRA) and promyelocytic leukemia/retinoic acid receptor alpha (PML-RARA) fusion assay, respectively. We present this case to remark on the novelty of these two acute diseases occurring together. Each of these entities is a hematologic emergency requiring immediate treatment before disease confirmation. We explore the mechanisms by which HIT occurs and outline the parameters for managing APL in the acute setting. Furthermore, this case serves to examine the treatment considerations for needing to carefully balance the thrombotic and hemorrhagic risk of both HIT and APL, which are clinically well-known for coagulopathy. Fortunately, HIT in this patient recovered on anticoagulation without bleeding or worsening thrombosis. Furthermore, following induction and consolidation treatment for APL, she remained negative for residual disease.

## Linked entities

- **Chemicals:** apixaban (PubChem CID 10182969)
- **Diseases:** heparin-induced thrombocytopenia (MONDO:0018048), acute promyelocytic leukemia (MONDO:0012883), pulmonary embolism (MONDO:0005279)

## Full-text entities

- **Genes:** PML (PML nuclear body scaffold) [NCBI Gene 5371] {aka MYL, PP8675, RNF71, TRIM19}, RARA (retinoic acid receptor alpha) [NCBI Gene 5914] {aka NR1B1, RAR, RARalpha}
- **Diseases:** APL (MESH:D015473), coagulopathy (MESH:D001778), hematologic emergency (MESH:D006402), Thrombocytopenia (MESH:D013921), acute diseases (MESH:D000208), HIT (MESH:C562865), acute pulmonary embolism (MESH:D011655), thrombosis (MESH:D013927), pancytopenia (MESH:D010198), bleeding (MESH:D006470)
- **Chemicals:** serotonin (MESH:D012701), Heparin (MESH:D006493), apixaban (MESH:C522181)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11122665/full.md

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Source: https://tomesphere.com/paper/PMC11122665